Key result
Apixaban does not mask factor V Leiden diagnosis, leaving APCR ratios lower in heterozygous patients.
Why the study?
Apixaban causes a false increase in APCR ratios and possibly protein S activity, raising the question of whether it can mask a diagnosis of factor V Leiden or protein S deficiency in patients undergoing hypercoagulation testing.
Does apixaban treatment interfere with activated protein C resistance (APCR) testing for factor V Leiden or protein S activity testing in patients undergoing hypercoagulation evaluation?
Observational (n=58)
Does apixaban treatment interfere with activated protein C resistance (APCR) testing for factor V Leiden or protein S activity testing in patients undergoing hypercoagulation evaluation?
p-value: p=<.001
Apixaban does not cause clinically significant interference with APCR testing for factor V Leiden or protein S activity, avoiding the need for indiscriminate reflex DNA testing in patients on the drug.
Apixaban may preserve APCR discrimination for factor V Leiden; leaves open reliability in routine hypercoagulability evaluations.
CONTEXT.—: Apixaban causes a false increase in activated protein C resistance (APCR) ratios and possibly protein S activity. OBJECTIVE.—: To investigate whether this increase can mask a diagnosis of factor V Leiden (FVL) or protein S deficiency in an actual population of patients undergoing apixaban treatment and hypercoagulation testing. DESIGN.—: During a 4.5-year period involving 58 patients, we compared the following 4 groups: heterozygous for FVL (FVL-HET)/taking apixaban, wild-type/taking apixaban, heterozygous for FVL/no apixaban, and normal APCR/no apixaban. Patients taking apixaban were also tested for protein S functional activity and free antigen (n = 40). RESULTS.—: FVL-HET patients taking apixaban had lower APCR ratios than wild-type patients (P < .001). Activated protein C resistance in FVL-HET patients taking apixaban fell more than 3 SD below the cutoff of 2.2 at which the laboratory reflexes FVL DNA testing. No cases of FVL were missed despite apixaban. In contrast to rivaroxaban, apixaban did not interfere with the assessment of protein S activity (mean activity 93.9 IU/dL, free antigen 93.1 IU/dL, P = .39). A total of 3 of 40 patients (8%) had low free protein S antigen (30, 55, and 57 IU/dL), with correspondingly similar activity results (27, 59, and 52 IU/dL, respectively). Apixaban did not cause a missed diagnosis of protein S deficiency. CONCLUSIONS.—: Despite apixaban treatment, APCR testing can distinguish FVL-HET from healthy patients, rendering indiscriminate FVL DNA testing of all patients on apixaban unnecessary. Apixaban did not affect protein S activity.
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Maryamchik et al. (2020) conducted an observational in Factor V Leiden or protein S deficiency testing (n=58). Apixaban vs. No apixaban / wild-type patients was evaluated on Activated protein C resistance (APCR) ratios (p=<.001). Apixaban exposure did not mask the diagnosis of factor V Leiden, as heterozygous patients on apixaban had significantly lower APCR ratios than wild-type patients (P<.001).
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